When it comes to vascular brain injury, the dementia field has been mired in uncertainty. What is it, exactly? How can scientists measure and treat it? How does it realted to Alzheimer's patholology or contribute to cognitive decline? Answers to these old questions are still lacking, but two recent studies published online February 11 and 18 in JAMA Neurology suggest that vascular damage and amyloid plaques occur independently in early stages of AD. William Jagust, University of California, Berkeley, and colleagues find that the pathologies are separate, and that only vascular injury tracks with cognitive decline. LIkewise, scientists led by Adam Brickman, Columbia University, New York, report that white matter hyperintensities and amyloid are independent risk factors for Alzheimer's disease (AD). These findings add to a growing body of literature suggesting that vascular causes of decline are distinct from amyloid pathology, and that they deserve their own spot at the dementia table.

"Vascular brain injury has typically taken on a secondary role in the hunt for what causes dementia in Alzheimer's disease," said Natalie Marchant, first author on the Jagust paper and how at the University of Sussex, U.K. "It is important to understand what A-beta does to cognition, but our study emphasizes that it is necessary to consider the impact of vascular brain injury, too."

A number of studies suggest a link between vascular risk factors and A-beta aggregation. For instance, acute hypoxia, such as that resulting from a stroke, leads to more A-beta production in mouse neurons.